Association of ApoE and HDL-C with cardiovascular and cerebrovascular disease:
potential benefits of LDL-apheresis therapy,
Clinical Lipidology, Future Medicine
June 2009, Vol. 4, No. 3, Pages 311-329 , DOI 10.2217/clp.09.21
Review
Patrick M Moriarty
ApoE forms a lipid–protein complex with HDL-cholesterols (HDL-C) and remnant lipoproteins and is an important regulator of cholesterol and lipid clearance, transport and distribution. In the CNS, ApoE is strictly bound to HDL.
Unlike ApoE2 or ApoE3, the ApoE4 isoform is associated with both coronary artery disease and Alzheimer’s disease.
HDL-C levels may possess a U-shaped association with vascular diseases and HDL-C size might reflect an alteration in function.
Inflammation plays a key role in coronary artery disease and Alzheimer’s disease.
Elevated inflammatory markers such as C-reactive protein and serum amyloid A are associated with both diseases. Serum amyloid A, similar to ApoE, binds to HDL-C and may alter the lipoproteins size and function.
Familial hypercholesterolemia (FH) is a genetic disorder resulting in elevated plasma levels of LDL-cholesterol (LDL-C), xanthomas and premature coronary artery disease. FH patient’s plasma contains decreased levels of HDL-C with increased levels of ApoE4 and ApoE-bound HDL.
LDL-apheresis therapy lowers LDL-C and is designated for FH patients resistant to pharmacotherapy.
LDL-apheresis also lowers inflammatory HDL-C, ApoE4, and a host of inflammatory markers such as C-reactive protein and serum amyloid A. LDL-apheresis, adjunct to reducing cholesterol, may provide additional benefit to patients with cardiovascular and cerebrovascular diseases.
potential benefits of LDL-apheresis therapy,
Clinical Lipidology, Future Medicine
June 2009, Vol. 4, No. 3, Pages 311-329 , DOI 10.2217/clp.09.21
Review
Association of ApoE and HDL-C with cardiovascular and cerebrovascular disease: potential benefits of LDL-apheresis therapy
ApoE forms a lipid–protein complex with HDL-cholesterols (HDL-C) and remnant lipoproteins and is an important regulator of cholesterol and lipid clearance, transport and distribution. In the CNS, ApoE is strictly bound to HDL.
Unlike ApoE2 or ApoE3, the ApoE4 isoform is associated with both coronary artery disease and Alzheimer’s disease.
HDL-C levels may possess a U-shaped association with vascular diseases and HDL-C size might reflect an alteration in function.
Inflammation plays a key role in coronary artery disease and Alzheimer’s disease.
Elevated inflammatory markers such as C-reactive protein and serum amyloid A are associated with both diseases. Serum amyloid A, similar to ApoE, binds to HDL-C and may alter the lipoproteins size and function.
Familial hypercholesterolemia (FH) is a genetic disorder resulting in elevated plasma levels of LDL-cholesterol (LDL-C), xanthomas and premature coronary artery disease. FH patient’s plasma contains decreased levels of HDL-C with increased levels of ApoE4 and ApoE-bound HDL.
LDL-apheresis therapy lowers LDL-C and is designated for FH patients resistant to pharmacotherapy.
LDL-apheresis also lowers inflammatory HDL-C, ApoE4, and a host of inflammatory markers such as C-reactive protein and serum amyloid A. LDL-apheresis, adjunct to reducing cholesterol, may provide additional benefit to patients with cardiovascular and cerebrovascular diseases.
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